English   español  
Please use this identifier to cite or link to this item: http://hdl.handle.net/10261/41894
Share/Impact:
Statistics
logo share SHARE logo core CORE   Add this article to your Mendeley library MendeleyBASE

Visualizar otros formatos: MARC | Dublin Core | RDF | ORE | MODS | METS | DIDL
Exportar a otros formatos:
Title

The persistence of infectious pancreatic necrosis virus and its influence on the early immune response

AuthorsRodríguez Saint-Jean, Sylvia ; Heras, Ana Isabel de las ; Pérez Prieto, Sara I.
KeywordsInfectious pancreatic necrosis virus (IPNV)
Oncorhynchus mykiss
Rainbow trout RTG-2 cell line
Birnaviridae Infections
Fish diseases
Double-stranded RNA virus
Fish viruses
IFN induction in IPNV
Issue DateJul-2010
PublisherElsevier
CitationVeterinary Immunology and Immunopathology, 136(1-2): 81-91 (2010)
AbstractPersistent infection by IPNV was induced in RTG-2 and RTG-P1 cells in vitro and the influence of this phenomenon on viral infectivity, viral antigen expression and interference with homologous and heterologous viruses was characterized over successive passages. The induction of IFN was also assessed, as was the sequence of the VP2 viral capsid protein, the region believed to be responsible for virulence, attenuation or persistence. Viral antigen expression was recorded in cells with no evidence of cytopathic effects and in these conditions, flow cytometry was more sensitive than RT-PCR to demonstrate the presence of a non-lytic virus. Interference of homologous viral infection could be detected in cross-infection experiments and in RTG-P1 cells persistently infected with IPNV, the Mx1 promoter could still be activated for at least 5 successive passages. Indeed, although over-induction of luciferase was not observed by re-infection with homologous or heterologous viruses, a significant increase in luciferase was induced by poly I:C. IFN transcripts could be quantified by qRT-PCR in the persistent cells at several passages, suggesting that IFN plays a role in maintaining IPNV persistence. In addition, we observed the same determinants in the VP2 sequences from the persistent virus as those described previously for IPNV adaptation and persistence in cell culture.
Publisher version (URL)http://dx.doi.org/10.1016/j.vetimm.2010.02.015
URIhttp://hdl.handle.net/10261/41894
DOI10.1016/j.vetimm.2010.02.015
ISSN0165-2427
E-ISSN1873-2534
Appears in Collections:(CIB) Artículos
Files in This Item:
There are no files associated with this item.
Show full item record
Review this work
 

Related articles:


WARNING: Items in Digital.CSIC are protected by copyright, with all rights reserved, unless otherwise indicated.